Early and sustained coronary artery patency after thrombolytic therapy has been implicated as one of the most important predictors of short and long term survival after acute myocardial infarction. Between 20% and 40% of patients receiving thrombolytic therapy fail to recanalize the infarct-related artery during the first few hours. Rescue angioplasty and selective infusion of fibrinolytic agents have been used successfully to restore patency of the infarct-related artery. Patients with successful rescue angioplasty have been noted to have similar long-term survival as patients who reperfuse after thrombolytic therapy alone, suggesting that procedures aimed at restoring patency after thrombolytic therapy has failed are beneficial in selected patients.
Acute coronary arteriography has to date been the only reliable method to identify patients who have failed to reperfuse. In the Thrombolysis Angioplasty in Myocardial Infarction (TAMI) 5 study a strategy using acute angiography coupled with rescue angioplasty was noted to be associated with a better overall clinical outcome after thrombolysis. However, performing acute angiography on all patients with acute myocardial infarction after thrombolysis is costly and not possible in most U.S. hospitals or in the world.
The critical importance of patency of the infarct-related artery for in-hospital and long-term survival has been documented by several studies. To non-invasively identify the subset of patients who have failed to restore patency or have incomplete reperfusion after intravenous thrombolytic therapy could allow these patients to undergo rescue angioplasty or more aggressive pharmacologic approaches.
Previous studies have examined clinical markers of reperfusion. These have included the resolution of chest pain or reperfusion arrhythmias occurring after thrombolysis. Arrhythmias have not been useful in three studies as a reliable marker of reperfusion, with sensitivities ranging between 37% and 63%. Resolution of chest pain has been a better marker of reperfusion, but has clinical disadvantages as patients perception of chest pain during myocardial infarction can be hard to interpret. Nevertheless, patients who have complete resolution of chest pain during thrombolytic therapy have a highly significant association with patency of the infarct-related artery (p=0.0005) documented during acute angiography. However, resolution of chest pain after thrombolysis is insufficient as the sole marker of reperfusion as only a small proportion of patients exhibit this phenomena.
A variety of intracellular components in the myocardium have been used to assess reperfusion. These markers have included myoglobin, myosin light chains, troponin T and both the MM and MB isoenzyme of creatine kinase (CK). Newly isolated tissue isoforms of CK-MB also hold promise as reliable predictors of reperfusion, but are limited by relative long assay time and lack of availability in most chemistry laboratories. In general these studies have examined the time to peak on the CK-MB release curve or used methods that require prolonged assay times. Both of these factors do not allow for early and rapid triage of patients after thrombolysis to enhance the care of patients who have failed to restore patency.